Amniotic fluid contains a high concentration of prolactin which is produced and secreted by the decidua. In vitro models have suggested that bacterial products inhibit prolactin secretion by decidual cells. To further examine this potentially important regulatory mechanism in the whole animal, chronically instrumented pregnant rhesus monkeys were prepared. Experimental infection was induced by intra-amniotic or choriodecidual innoculation of 103- 106 Group B streptococci. In addition, IL-1 was infused into the amniotic cavity to test the hypothesis that inflammatory cytokines were mediating the effect of bacterial infection. Serial amniotic fluid samples were obtained prior to and following innoculation or infusion of Il-1 . The average prolactin level prior to innoculation (0 hours) equaled 34.0q6.4 g/ml. There was a 40% decrease in prolactin by 37 hours post-infection (n=6). In 3 animals with later delivery, prolactin levels decreased by 71% between 61-72 hours post-infection (p < 0.01 versus preinfection). Histopathology confirmed chorioamnionitis and deciduitis. Infusion of IL-1 also caused a decrease in amniotic fluid prolactin. There was a 42% decrease in prolactin between 0-24 hours post-infusion (p<0.05) and a 66% decrease between 25-72 hours after IL-1 infusion (p<0.05; n=6). In summary, intrauterine bacterial infection decreases amniotic fluid prolactin prior to pre-term labor and IL-1 mimics this effect. These results are consistent with previous observations in vitro and they offer the first report in vivo of a potential relationship between infection and amniotic fluid prolactin.